Hypercholesterolemia: Waters DD

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A digest of articles written 1999 and later, on the topic "Hypercholesterolemia," originating from Planet Earth —» Waters DD.  Display:  All Citations ·  All Abstracts
1 Guideline Reassessment of National Cholesterol Education Program Adult Treatment Panel-III guidelines: one year later. 2002

Ansell BJ, Waters DD, Anonymous00316. · No affiliation provided · Am J Cardiol. · Pubmed #12208415 No free full text.

This publication has no abstract.

2 Review What is the role of intensive cholesterol lowering in the treatment of acute coronary syndromes? 2001

Waters DD, Hsue PY. · Division of Cardiology, San Francisco General Hospital, San Francisco, California 94110, USA. · Am J Cardiol. · Pubmed #11595193 No free full text.

Abstract: Cholesterol lowering with statins reduces coronary events in a primary-prevention setting and in patients with stable coronary disease. However, where the risk of a coronary event is highest, in the early months after an episode of unstable angina or non-Q-wave infarction, the effect of statin therapy has not been evaluated until recently. The lack of an early benefit in the 3 main statin trials in stable coronary disease may have discouraged this type of investigation. Yet, evidence suggests that intensive cholesterol lowering can rapidly influence several mechanisms intimately related to the pathogenesis of acute coronary syndromes; specifically, improvement in endothelial function, decreased propensity for platelet thrombus formation, and reduced inflammation. Furthermore, 3 nonrandomized, observational studies have recently reported an improved outcome in statin-treated compared with untreated patients after acute coronary syndromes.

3 Review Are we aggressive enough in lowering cholesterol? 2001

Waters DD. · Cardiology Division, Department of Medicine, San Francisco General Hospital, San Francisco, California 94110, USA. · Am J Cardiol. · Pubmed #11520481 No free full text.

Abstract: To date, 5 major randomized, placebo-controlled statin trials--the Scandinavian Simvastatin Survival Study, West of Scotland Coronary Prevention Study, Cholesterol and Recurrent Events trial, Long-term Intervention with Pravastatin in Ischaemic Disease, and Air Force/Texas Coronary Atherosclerosis Prevention Study--have convincingly shown that total mortality and major coronary events can be significantly reduced by lowering levels of low-density lipoprotein cholesterol (LDL-C) with statin therapy. These results were achieved in a broad range of patients including those with and without a history of coronary artery disease and with elevated or average LDL-C levels. The results also support the large body of epidemiologic evidence demonstrating that the lower the cholesterol level, the lower the cardiovascular risk. Evidence now substantially supports the urgency of physicians to aggressively target the lowering of LDL-C levels for the primary and secondary prevention of coronary disease.

4 Review What do the statin trials tell us? 2001

Waters DD. · Division of Cardiology, San Francisco General Hospital, University of California at San Francisco, 94110, USA. · Clin Cardiol. · Pubmed #11501601 No free full text.

Abstract: The results of five large-scale, randomized, placebo-controlled trials, involving nearly 31,000 subjects, attest to the benefits of statins in the prevention of coronary events. Several key observations can be made on the basis of the evidence from these investigations. Of primary importance is the fact that statins reduce coronary event rates in patients with or without coronary heart disease. The percentage reduction in risk increases with each successive year of statin therapy. Moreover, the risk reduction is proportional to the reduction in low-density lipoprotein cholesterol. Subgroup analyses have demonstrated that the efficacy of statins extends to specific subgroups of patients, including women, people with diabetes, and older individuals. These agents also reduce the risk of stroke and transient ischemic attacks in patients with coronary disease. Both the randomized trials and widespread clinical experience have confirmed that statins are safe and do not increase the risk of cancer or mortality. Several markers of atherosclerotic risk are ameliorated by statins, although the clinical significance of this observation remains under investigation. The broad range of the therapeutic effects of statins yields safe, effective management of hypercholesterolemia in current practice while also providing a foundation for additional therapeutic refinements in the future.

5 Review What do the statin trials tell us? free! 2001

Waters DD. · No affiliation provided · Am J Manag Care. · Pubmed #11383375 links to  free full text

Abstract: The results of 5 major placebo-controlled trials evaluating the effects of statins in approximately 31,000 individuals with and without known coronary disease have demonstrated the following: statins reduce the incidence of coronary events, the reduction in relative risk for coronary events increases with the duration of therapy, the reduction in coronary events is proportional to the reduction in low-density lipoprotein cholesterol (LDL-C) levels, and lower LDL-C levels are associated with lower event rates. The studies have also shown that statins are safe and effective in reducing the incidence of coronary events in women, individuals with diabetes, and patients older than 65 years of age and in reducing the risk of stroke and transient ischemic attacks in patients with coronary disease. Finally, studies indicate that statins ameliorate a variety of pathophysiologic processes that are associated with increased risk for atherosclerosis.

6 Clinical Conference Differences in medical care and disease outcomes among black and white women with heart disease. free! 2003

Jha AK, Varosy PD, Kanaya AM, Hunninghake DB, Hlatky MA, Waters DD, Furberg CD, Shlipak MG. · Division of General Medicine, San Francisco VA Medical Center, San Francisco, USA. · Circulation. · Pubmed #12939228 links to  free full text

Abstract: BACKGROUND: The risk of cardiovascular mortality is higher among black women than white women, and the reasons for this disparity are largely unexplored. We sought to evaluate differences in medical care and clinical outcomes among black and white women with established coronary artery disease. METHODS AND RESULTS: Among the 2699 women enrolled in the Heart and Estrogen/progestin Replacement Study (HERS), we used Cox proportional hazards models to determine the association of race with risk of coronary heart disease (CHD) events independent of major cardiovascular risk factors or medical therapies. During an average of 4.1 years of follow-up, CHD events were twice as likely in black compared with white women (6.4 versus 3.1 per 100 person-years, hazard ratio, 2.1; 95% confidence interval, 1.5 to 2.8; P<0.001). Black women had higher rates of hypertension, diabetes, and hypercholesterolemia, yet were less likely to receive aspirin or statins. Black women less often had optimal blood pressure (56% versus 63%; P=0.01) and LDL cholesterol (30% versus 38%; P=0.04) control at baseline and during follow-up. After adjusting for these and other differences, black women still had >50% higher CHD event risk (hazard ratio, 1.52; 95% confidence interval, 1.1 to 2.1; P=0.03). CONCLUSIONS: In a large cohort of women with heart disease, black women less often received appropriate preventive therapy and adequate risk factor control despite a greater CHD event risk. Interventions to improve appropriate therapy and risk factor control in all women, and especially black women, are needed.

7 Clinical Conference The effects of hydroxy-methyl-glutaryl co-enzyme A reductase inhibitors on platelet thrombus formation. 2002

Thompson PD, Moyna NM, White CM, Weber KM, Giri S, Waters DD. · Section of Preventive Cardiology, Division of Cardiology, Hartford Hospital, 80 Seymour Street, Hartford, CT 06102, USA. · Atherosclerosis. · Pubmed #11888512 No free full text.

Abstract: BACKGROUND: Hydroxy-methyl-glutaryl co-enzyme A reductase inhibitors (HMG CoA RIs) markedly improve the lipid profile of patients with hypercholesterolemia, but the magnitude and time course of the effect of these drugs on other risk factors for atherosclerosis are not well defined. METHODS: We employed a random assignment, double-blind design to compare the effect of 8 weeks of HMG CoA RI therapy with either pravastatin (40 mg QD; n=12) or simvastatin (20 mg QD; n=12) with placebo (n=13) on serum lipids, platelet thrombus formation (PTF), and markers of inflammation and thrombosis in patients with coronary artery disease. PTF was measured using a validated ex vivo perfusion chamber system. RESULTS: Total and LDL cholesterol decreased 20.3 +/- 12.7% and 31.4 +/- 16.5% in the HMG CoA RI group and were unchanged with placebo (P<0.01). Triglycerides also decreased 15.3 +/- 22.5% with HMG CoA RI therapy, but increased 8.4 +/- 30.0% with placebo (P=0.01). PTF increased 54.1 +/- 89.0% with placebo and decreased 8.0 +/- 46.82% with HMG CoA RI treatment (P<0.01). CONCLUSIONS: HMG CoA RI therapy with pravastatin or simvastatin reduces PTF after only 8 weeks of therapy. Such lipid effects may contribute to the prompt reduction in cardiovascular events noted in some clinical trials.